Despite the benefits of resistance, susceptibility to infectious disease is commonplace. Although specific susceptibility may be considered an inevitable consequence of the co-evolutionary arms race between parasite and host, a more general constraint may arise from the cost of an immune response. This “cost” hypothesis predicts a tradeoff between immune defense and other components of fitness. In particular, a tradeoff between immunity and sexually selected male behavior has been proposed. Here we provide experimental support for the direct phenotypic tradeoff between sexual activity and immunity by studying the antibacterial immune response inDrosophila melanogaster. Males exposed to more females showed a reduced ability to clear a bacterial infection, an effect that we experimentally link to changes in sexual activity. Our results suggest immunosuppression is an important cost of reproduction and that immune function and levels of disease susceptibility will be influenced by sexual selection.

Emerging plant diseases frequently have significant economic, environmental, cultural, and social impacts. The prediction of new disease emergence, associated with new pathogens or not, remains a difficult and controversial topic. The main factors driving epidemics are often only identified several years after outbreaks, generally revealing that a limited number of factors are associated with the emergence of specific groups of pathogens. This pattern is illustrated in the insect-borne xylem-limited bacterium Xylella fastidiosa, an organism associated with several new plant diseases in different regions of the globe. Research during the last decade focusing on several severe disease outbreaks has led to substantial changes in our understanding of X. fastidiosa biology, ecology, and evolution. This new information has not only led to new insights into aspects of the biology of this bacterium and its interactions with plant and insect hosts, but also made available a phylogenetic framework that has allowed for better inferences concerning factors leading to the emergence of diseases. Here we identify and discuss these main pathways leading to epidemics caused by X. fastidiosa. Our ultimate goal was to raise critical questions and issues for academics and regulatory agencies alike, since the information generated during the last decade has both raised new questions but also clarified old ones.